Ischemia is a leading cause of mortality and involves oxygen starvation of the myocardium. Unfortunately, many episodes of myocardial ischemia do not cause excessive pain or other noticeable warning signs and often go undetected. If left untreated, myocardial ischemia can lead to the symptoms associated with acute coronary syndrome and the eventual cell death associated with acute myocardial infarction. Acute coronary syndrome generally includes the clinical symptoms associated with unstable angina, non-ST segment elevation or non-Q-wave myocardial infarction, and ST segment elevation or Q-wave myocardial infarction. In patients with ventricular dysfunction, sustained ischemia can also trigger sudden cardiac death and/or myocardial decompensation. Early detection of myocardial ischemia provides the opportunity for a wide range of effective therapies such as surgical revascularization, neural stimulation, and drug delivery to reduce cardiac workload or improve cardiac circulation.
An electrocardiogram (ECG) or electrogram (EGM) presents a PQRST waveform sequence that characterizes the cyclical cardiac activity of a patient. The ST segment, which is associated with the repolarization of the ventricles, is typically close in amplitude to the baseline (i.e., isoelectric amplitude) of the signal sensed between consecutive PQRST sequences. During episodes of myocardial ischemia, the ST segment amplitude deviates from the baseline. Accordingly, deviation in the ST segment is often used to identify an occurrence of myocardial ischemia.
The T-wave from the PQRST sequences can also correlate with ischemic conditions. Variations in the T-wave, called T-wave alternans (TWA) are rate dependent and occur once an increase in heart rate exceeds the kinetics of intracellular calcium cycling. Thus, TWA can occur during myocardial ischemia due to coronary occlusion (supply ischemia) or when blood demand surpasses blood supply (demanding ischemia). Also, TWA directly reflect the development of an arrhythmogenic substrate for ventricular tachyarrhythmia (VT/VF) through the mechanism of repolarization dispersion and creating unidirectional conduction for reentry formation.